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      International Journal of COPD (submit here)

      This international, peer-reviewed Open Access journal by Dove Medical Press focuses on pathophysiological processes underlying Chronic Obstructive Pulmonary Disease (COPD) interventions, patient focused education, and self-management protocols. Sign up for email alerts here.

      39,063 Monthly downloads/views I 2.893 Impact Factor I 5.2 CiteScore I 1.16 Source Normalized Impact per Paper (SNIP) I 0.804 Scimago Journal & Country Rank (SJR)

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      Contributions of cardiovascular risk and smoking to chronic obstructive pulmonary disease (COPD)-related changes in brain structure and function

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          Abstract

          Background

          Brain damage and cardiovascular disease are extra-pulmonary manifestations of chronic obstructive pulmonary disease (COPD). Cardiovascular risk factors and smoking are contributors to neurodegeneration. This study investigates whether there is a specific, COPD-related deterioration in brain structure and function independent of cardiovascular risk factors and smoking.

          Materials and methods

          Neuroimaging and clinical markers of brain structure (micro- and macro-) and function (cognitive function and mood) were compared between 27 stable COPD patients (age: 63.0±9.1 years, 59.3% male, forced expiratory volume in 1 second [FEV 1]: 58.1±18.0% pred.) and 23 non-COPD controls with >10 pack years smoking (age: 66.6±7.5 years, 52.2% male, FEV 1: 100.6±19.1% pred.). Clinical relationships and group interactions with brain structure were also tested. All statistical analyses included correction for cardiovascular risk factors, smoking, and aortic stiffness.

          Results

          COPD patients had significantly worse cognitive function ( p=0.011), lower mood ( p=0.046), and greater gray matter atrophy ( p=0.020). In COPD patients, lower mood was associated with markers of white matter (WM) microstructural damage ( p<0.001), and lower lung function (FEV 1/forced vital capacity and FEV 1) with markers of both WM macro ( p=0.047) and microstructural damage ( p=0.028).

          Conclusion

          COPD is associated with both structural (gray matter atrophy) and functional (worse cognitive function and mood) brain changes that cannot be explained by measures of cardiovascular risk, aortic stiffness, or smoking history alone. These results have important implications to guide the development of new interventions to prevent or delay progression of neuropsychiatric comorbidities in COPD. Relationships found between mood and microstructural abnormalities suggest that in COPD, anxiety, and depression may occur secondary to WM damage. This could be used to better understand disabling symptoms such as breathlessness, improve health status, and reduce hospital admissions.

          Most cited references46

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          Prevalence and outcomes of diabetes, hypertension and cardiovascular disease in COPD.

          D Mannino, D. Thorn, A Swensen … (2008)
          Chronic obstructive pulmonary disease (COPD) is associated with important chronic comorbid diseases, including cardiovascular disease, diabetes and hypertension. The present study analysed data from 20,296 subjects aged > or =45 yrs at baseline in the Atherosclerosis Risk in Communities Study (ARIC) and the Cardiovascular Health Study (CHS). The sample was stratified based on baseline lung function data, according to modified Global Initiative for Obstructive Lung Disease (GOLD) criteria. Comorbid disease at baseline and death and hospitalisations over a 5-yr follow-up were then searched for. Lung function impairment was found to be associated with more comorbid disease. In logistic regression models adjusting for age, sex, race, smoking, body mass index and education, subjects with GOLD stage 3 or 4 COPD had a higher prevalence of diabetes (odds ratio (OR) 1.5, 95% confidence interval (CI) 1.1-1.9), hypertension (OR 1.6, 95% CI 1.3-1.9) and cardiovascular disease (OR 2.4, 95% CI 1.9-3.0). Comorbid disease was associated with a higher risk of hospitalisation and mortality that was worse in people with impaired lung function. Lung function impairment is associated with a higher risk of comorbid disease, which contributes to a higher risk of adverse outcomes of mortality and hospitalisations.
          Article 0 comments Cited 345 times – based on 0 reviews     Review now
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            Mortality in COPD: Role of comorbidities.

            D Sin, N R Anthonisen, J. Soriano … (2006)
            Chronic obstructive pulmonary disease (COPD) represents an increasing burden throughout the world. COPD-related mortality is probably underestimated because of the difficulties associated with identifying the precise cause of death. Respiratory failure is considered the major cause of death in advanced COPD. Comorbidities such as cardiovascular disease and lung cancer are also major causes and, in mild-to-moderate COPD, are the leading causes of mortality. The links between COPD and these conditions are not fully understood. However, a link through the inflammation pathway has been suggested, as persistent low-grade pulmonary and systemic inflammation, both known risk factors for cardiovascular disease and cancer, are present in COPD independent of cigarette smoking. Lung-specific measurements, such as forced expiratory volume in one second (FEV(1)), predict mortality in COPD and in the general population. However, composite tools, such as health-status measurements (e.g. St George's Respiratory Questionnaire) and the BODE index, which incorporates Body mass index, lung function (airflow Obstruction), Dyspnoea and Exercise capacity, predict mortality better than FEV(1) alone. These multidimensional tools may be more valuable because, unlike predictive approaches based on single parameters, they can reflect the range of comorbidities and the complexity of underlying mechanisms associated with COPD. The current paper reviews the role of comorbidities in chronic obstructive pulmonary disease mortality, the putative underlying pathogenic link between chronic obstructive pulmonary disease and comorbid conditions (i.e. inflammation), and the tools used to predict chronic obstructive pulmonary disease mortality.
            Article 0 comments Cited 265 times – based on 0 reviews     Review now
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              Prospective evaluation of a method for estimating ascending aortic pressure from the radial artery pressure waveform.

              A Pauca, M F O'Rourke, N Kon (2001)
              Pressure wave reflection in the upper limb causes amplification of the arterial pulse so that radial systolic and pulse pressures are greater than in the ascending aorta. Wave transmission properties in the upper limbs (in contrast to the descending aorta and lower limbs) change little with age, disease, and drug therapy in adult humans. Such consistency has led to use of a generalized transfer function to synthesize the ascending aortic pressure pulse from the radial pulse. Validity of this approach was tested for estimation of aortic systolic, diastolic, pulse, and mean pressures from the radial pressure waveform. Ascending aortic and radial pressure waveforms were recorded simultaneously at cardiac surgery, before initiation of cardiopulmonary bypass, with matched, fluid-filled manometer systems in 62 patients under control conditions and during nitroglycerin infusion. Aortic pressure pulse waves, generated from the radial pulse, showed agreement with the measured aortic pulse waves with respect to systolic, diastolic, pulse, and mean pressures, with mean differences <1 mm Hg. Control differences in Bland-Altman plots for mean+/-SD in mm Hg were systolic, 0.0+/-4.4; diastolic, 0.6+/-1.7; pulse, -0.7+/-4.2; and mean pressure, -0.5+/-2.0. For nitroglycerin infusion, differences respectively were systolic, -0.2+/-4.3; diastolic, 0.6+/-1.7; pulse, -0.8+/-4.1; and mean pressure, -0.4+/-1.8. Differences were within specified limits of the Association for the Advancement of Medical Instrumentation SP10 criteria. In contrast, differences between recorded radial and aortic systolic and pulse pressures were well outside the criteria (respectively, 15.7+/-8.4 and 16.3+/-8.5 for control and 14.5+/-7.3 and 15.1+/-7.3 mm Hg for nitroglycerin). Use of a generalized transfer function to synthesize radial artery pressure waveforms can provide substantially equivalent values of aortic systolic, pulse, mean, and diastolic pressures.
              Article 0 comments Cited 209 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Chron Obstruct Pulmon Dis
                Journal ID (iso-abbrev): Int J Chron Obstruct Pulmon Dis
                Journal ID (publisher-id): COPD
                Journal ID (pmc): copd
                Title: International Journal of Chronic Obstructive Pulmonary Disease
                Publisher: Dove
                ISSN (Print): 1176-9106
                ISSN (Electronic): 1178-2005
                Publication date (Electronic): 21 August 2019
                Publication date Collection: 2019
                Volume: 14
                Pages: 1855-1866
                Affiliations
                [1 ]Institute for Molecular and Clinical Sciences, St George’s University of London , London SW17 ORE, UK
                [2 ]Institute for Infection and Immunity, St George’s University of London , London SW17 ORE, UK
                [3 ]Clinical Research and Imaging Centre, University of Bristol , Bristol BS2 8DX, UK
                [4 ]Academic Respiratory Unit, University of Bristol , Bristol BS10 5NB, UK
                Author notes
                Correspondence: James W DoddAcademic Respiratory Unit, University of Bristol , Learning & Research Building Southmead Hospital, BristolBS10 5NB, UKTel +44 117 414 1276Email james.dodd@bristol.ac.uk
                Author information
                http://orcid.org/0000-0002-6908-5079
                http://orcid.org/0000-0001-8797-6855
                http://orcid.org/0000-0002-6128-9202
                http://orcid.org/0000-0001-6125-7326
                http://orcid.org/0000-0002-0871-3721
                http://orcid.org/0000-0001-6087-9182
                http://orcid.org/0000-0003-4805-5759
                Article
                Publisher ID: 213607
                DOI: 10.2147/COPD.S213607
                PMC ID: 6709516
                PubMed ID: 31686798
                SO-VID: d092250e-0d97-4b2a-9c9e-60fa60e143e1
                Copyright © © 2019 Spilling et al.
                License:

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                Date received : 26 April 2019
                Date accepted : 10 July 2019
                Page count
                Figures: 2, Tables: 2, References: 73, Pages: 12
                Categories
                Subject: Original Research

                ScienceOpen disciplines: Respiratory medicine
                Keywords: chronic lung disease,cigarette smoke,cognition,depression,mri,neuroimaging
                Data availability:
                ScienceOpen disciplines: Respiratory medicine
                Keywords: chronic lung disease, cigarette smoke, cognition, depression, mri, neuroimaging

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